Our hypothesis is that interleukin-1 (IL-1) induced neutrophil recruitment and activation with release of damaging oxygen radicals (02*) and/or elastase is a fundamental feature of ARDS. We propose that endotoxin (LPS) and IL-1 initiate neutrophil recruitment and activation by production of LTB4, IL-8 and increased xanthine oxidase (XO) activity leading to superoxide (O2) activated chemotaxins. Activated neutrophils inflict oxidative damage reflected by glutathione oxidation, antiprotease inactivation, vitamin E depletion and lipid peroxidation. These events cause acute lung injury, kidney damage, more neutrophil influx and lacerations in neutrophils. Concomitant increases in markers (MnSOD, catalase, GSSG, MPO, elastase-alpha1Pi complexes, and H202 and other factors) reflect and impact ARDS progression.